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Figure 2 | Chinese Journal of Cancer

Figure 2

From: Selective killing of K-ras–transformed pancreatic cancer cells by targeting NAD(P)H oxidase

Figure 2

Capsaicin caused preferential reactive oxygen species (ROS) accumulation and selectively inhibited NOX activity in K-ras –transformed E6E7 cells. A, incubation with 1 μmol/L capsaicin for 12 hours caused tremendous ROS accumulation in K-ras–transformed cells as compared with untreated K-ras–transformed cells (superoxide mean level, 16 vs. 53). B, the same treatment caused a minimum effect on ROS production in E6E7 cells as compared with untreated parental E6E7 cells (superoxide mean level, 8 vs. 9). C, the dose-dependent increase in superoxide generation induced by capsaicin in parental and K-ras–transformed E6E7 cells. D, treatment with 10 μmol/L capsaicin caused a significant increase in both SOD1 and SOD2 in K-ras–transformed cells. E, total cell lysates of untreated parental E6E6 cells, untreated K-ras–transformed E6E6 cells, and K-ras–transformed E6E6 cells treated with 10 μmol/L capsaicin for 12 hours were pulled down with nucleotide-free Rac1 G15A agarose beads. The precipitated active Rac was detected by anti–Rac-GEF antibody. F, E6E7 and K-ras–transformed cells were pretreated with 10 μmol/L capsaicin for 12 hours. NOX activity was measured in the presence of 100 μmol/L NADPH by lucigenin-derived chemiluminescence in the plasma membrane fraction of parental and K-ras–transformed E6E7 cells, with or without capsaicin treatment. The values are shown as the mean ± SD. **, P < 0.01.

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